Endogenous nitric oxide is involved in post-ischemic functional recovery induced by adenosine-enhanced ischemic preconditioning.

2003 Fiscal Year Final Research Report Summary

• Project/Area Number: 13671397
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Thoracic surgery
• Research Institution: University of Miyazaki(Miyazaki Medical College)
• Principal Investigator: YANO Mitsuhiro Miyazaki Medical College, The 2nd. Department of Surgery, Surgical Assistant, 医学部, 助手 (00305096)
• Co-Investigator(Kenkyū-buntansha): ONITSUKA Toshlo Miyazaki Medical College, The 2nd. Department of Surgery, Professor, 医学部, 教授 (60108595) ; NAKAMURA Kunihide Miyazaki Medical College, The 2nd. Department of Surgery, Lecturer, 医学部, 講師 (10207871)
• Project Period (FY): 2001 – 2003
• Keywords: Adenosine-enhansed Ischemic Preconditioning / Ischemia-Reperfusion Injury / Cardioprotection / nitric oxide / Isolated Heart Perfusion

Research Abstract

The precise mechanism of cardioprotection afforded by adenosine-enhanced ischemic preconditioning (APC) remains unknown. The present study examines whether endogenous nitric oxide (NO) contributes to post-ischemic functional recovery during early reperfusion in the rabbit heart treated by APC. Langendorff perfused hearts underwent global ischemia for 30 minutes followed by reperfusion for 120 minutes. Hemodynamic parameters and NO concentrations were determined during reperfusion. The hearts were separated into groups as follows : perfusion without global ischemia for 180 minutes (Control) ; global ischemia and reperfusion (GI group) ; 5 minutes of global ischemia followed by 5 minutes of reperfusion then 30 minutes of global ischemia and 120 minutes of reperfusion (ischemic preconditioned (IPC) group) ; a 10 ml bolus injection of 1 mmol/L adenosine immediately before IPC (APC group) ; APC plus NG -Nitro-L-arginine methyl ester (L-NAME) for first 30 minutes of reperfusion (L-NAME group). The first derivative of left ventricular pressure, left ventricular end-diastolic pressure and coronary flow were significantly improved in the APC group as compared with the GI and IPC groups (p < 0.05). The NO concentration was significantly increased in the APC group compared with the other groups after 10 minutes of reperfusion (p < 0.05). These effects were abolished by NO synthase inhibition using L-NAME. Our results suggested that endogenous NO is involved in the post-ischemic functional recovery of the heart afforded by APC.